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Mitral Valve Prolapse And Panic Attacks/Anxiety

Permission graciously given by the author to reproduce this paper
Mitral Valve Prolapse And Panic Attacks/Anxiety Dysautonomias

Reference:  Much of the information for this paper was taken from the:
National Dysautonomia Research Foundation
1407 W Fourth Street, Suite 160, Red Wing, MN 55066-2108
Phone: (651) 267-0525  Fax: (651) 267-0524

NDRF is pleased to make available the NDRF Handbook for Patients with Dysautonomias, written by Dr. David S. Goldstein, MD, PhD and Linda J. Smith.  This in-depth guidebook for patients has been made possible with the support of the Medtronic Foundation.

Mitral valve prolapse is a disorder in which the heart's mitral valve -- which separates the left upper chamber (atrium) from the left lower chamber (ventricle) -- billows out and does not close properly.

Panic Attack: Panic attack may be another symptom of MVP. A panic attack is a sudden feeling of intense anxiety or impending doom for no apparent reason. A panic attack may be mild or severe and disabling. At least four of the following symptoms appear during an attack:

• Dyspnea
• Palpitations
• Chest pain and discomfort
• Sensation of being choked or smothered
• Feelings of dizziness, vertigo, or unsteadiness
• Paresthesias
• Hot and cold flashes; sweating; faintness
• Trembling or shaking
• Fear of dying, going crazy, or uncontrolled behavior

While many recognize a connection between panic attacks and Mitral Valve Prolapse (MVP), they often cannot explain this connection. Researchers into this problem believe the connection is actually a dysfunction in the Autonomic Nervous System (ANS). 

Dysautonomia: The ANS controls the involuntary system of the body such as heart beat, blood pressure, body temperature, intestinal functions, sweating, etc. The system is made of two parts: the sympathetic (the "accelerator") and the parasympathetic (the "brakes"). When these two are out of balance or go awry, it is described as dysautonomia.  Other terminology that is used includes - Autonomic Dysfunction, Autonomic Failure and Autonomic Neuropathy.

There are many types of dysautonomia and "Mitral Valve Prolapse Syndrome/Dysautonomia" is one of them. The name seems to indicate maybe the problem is with MVP when actually MVP is just one of the myriad of symptoms of MVP SYNDROME/DYSAUTONOMIA. 

These symptoms can include: 

•    Mitral Valve Prolapse (in 2/3 of patients) 
•    Anxiety and/or panic attacks 
•    Depression and/or mood swings 
•    Chest discomfort or pain 
•    Palpitations or feelings of skipped heart beats or flip-flops 
•    Dizziness and/or unsteadiness 
•    Almost passing out (presyncope) or passing out (syncope) 
•    Pallor or redness of extremities 
•    Malaise, a general sense of being ill 
•    Weakness, fatigue and/or loss of stamina 
•    Inability to tolerate heat or sun for long 
•    Gastrointestinal problems 
•    Headaches or migraines 
•    Numbness and/or tingling in the extremities 

The Amygdala:  Anxiety disorder, panic attacks (anxiety attacks), phobia, OCD & PTSD sufferer has a condition that is caused and perpetuated by the Amygdala (Am-ig-da-la) ; it's a small almond shaped organ (colored red in drawying below) in the brain and is part of the Lymbic System. 

Source: University of Washington Digital Anatomist Program 

The Amygdala controls anxiety levels. No matter how bad the symptoms are, no matter how long someone has had anxiety disorder, or how severe the panic attacks are, this tiny organ is responsible.  Stress, bereavement and life circumstances are just the triggers or catalysts for the anxiety - the Amygdala is THE cause! 

Anxiety disorder and panic attacks are caused by a tiny change in the way the brain handles anxiety signals from the sensory organs.  The “anxiety switch”, (the Amygdala), is either “anxiety ON” or “anxiety OFF”; when the switch is anxiety off it can be activated only by real danger, when it becomes “stuck on” it can produce anxiety disorder symptoms, panic attacks, OCD, PTSD and phobias.  The Amygdala has become “re-set” at a higher “resting” level of anxiety and it is this that causes these conditions. 

Many believe this 're-set' happens through Operant Conditioning - it's the same process that happens when you learn new activities - like driving or playing an instrument - it's learning through repetition.

This is why the slightest anxious thought or sensation can send one into anxiety and/or panic attacks mode. It is why one cannot cope with normal situations like they use to, it is why one may have constant anxiety disorder symptoms or panic attacks (anxiety attacks).  The reactions that happen in the brain are not wrong - they just occur inappropriately!

What follows are abstracts that comment directly on the role of the Amygdala in anxiety.  This list is not intended to be exhaustive but rather is a sample of the available literature. 

1. Wallace TL; Stellitano KE; Neve RL; Duman RS.  Effects of cyclic adenosine monophosphate response element binding protein overexpression in the basolateral amygdala on behavioral models of depression and anxiety. Biol Psychiatry 2004 Aug 1;56(3):151-60 

Abstract: BACKGROUND: Chronic antidepressant administration increases the cyclic adenosine monophosphate response element binding protein (CREB) in the amygdala, a critical neural substrate involved in the physiologic responses to stress, fear, and anxiety. METHODS: To determine the role of CREB in the amygdala in animal models of depression and anxiety, a viral gene transfer approach was used to selectively express CREB in this region of the rat brain. RESULTS: In the learned helplessness model of depression, induction of CREB in the basolateral amygdala after training decreased the number of escape failures, an antidepressant response. However, expression of CREB before training increased escape failures, and increased immobility in the forced swim test, depressive effects. Expression of CREB in the basolateral amygdala also increased behavioral measures of anxiety in both the open field test and the elevated plus maze, and enhanced cued fear conditioning. CONCLUSIONS: Taken together, these data demonstrate that CREB expression in the basolateral amygdala influences behavior in models of depression, anxiety, and fear. Moreover, in the basolateral amygdala, the temporal expression of CREB in relation to learned helplessness training, determines the qualitative outcome in this animal model of depression.

2. McHugh SB; Deacon RM; Rawlins JN; Bannerman DM.  Amygdala and ventral hippocampus contribute differentially to mechanisms of fear and anxiety. Behav Neurosci 2004 Feb;118(1):63-78 

Abstract:  Cytotoxic ventral hippocampal lesions produced anxiolytic effects on 4 ethologically based, unconditioned tests of anxiety in the rat (hyponeophagia, black/white 2-compartment box test, a successive alleys test that represents a modified version of the elevated plus-maze, and a social interaction test). Dorsal hippocampal lesions did not produce anxiolytic effects on these tests, suggesting a distinct specialization of function within the hippocampus. Furthermore, the effects of ventral hippocampal lesions were also distinct from those of amygdala lesions. This suggests that the effects of ventral hippocampal lesions are not simply due to direct or indirect effects on the amygdala, and that these 2 brain areas contribute differentially to a brain system (or systems) associated with the processing of fearful and/or anxiogenic stimuli.

3. Rauch SL; Shin LM; Wright CI.  Neuroimaging studies of amygdala function in anxiety disorders.  Ann N Y Acad Sci 2003 Apr;985:389-410

Abstract:  Neuroimaging research has helped to advance neurobiological models of anxiety disorders. The amygdala is known to play an important role in normal fear conditioning and is implicated in the pathophysiology of anxiety disorders. The amygdala may also be a target for the beneficial effects of cognitive-behavioral and medication treatments for anxiety disorders. In the current paper, we review neuroimaging research pertaining to the role of the amygdala in anxiety disorders and their treatment. Moreover, we discuss the development of new neuroimaging paradigms for measuring aspects of amygdala function, as well as the function of related brain regions. We conclude that such tools hold great promise for facilitating progress in relevant basic neuroscience as well as clinical research domains.

4. Amaral DG.  The primate amygdala and the neurobiology of social behavior: implications for understanding social anxiety.  Biol Psychiatry 2002 Jan 1;51(1):11-7 

Abstract:  The amygdala has long been implicated in the mediation of emotional and social behaviors. Because there are very few human subjects with selective bilateral damage of the amygdala, much of the evidence for these functional associations has come from studies employing animal subjects. Macaque monkeys live in complex, highly organized social groups that are characterized by stable and hierarchical relationships among individuals who engage in complex forms of social communication, such as facial expressions. Understanding the role of the amygdala in animals that display a level of social sophistication approaching that of humans will help in understanding the amygdala's role in human social behavior and in psychopathology such as social anxiety. Selective bilateral lesions of the amygdala in mature macaque monkeys result in a lack of fear responses to inanimate objects and a "socially uninhibited" pattern of behavior. These results imply that the amygdala functions as a protective "brake" on engagement of objects or organisms while an evaluation of potential threat is carried out. They also suggest that social anxiety may be a dysregulation or hyperactivity of the amygdala's evaluative process. Finally, recent data from developmental studies raise the possibility that, at least at some developmental stages, fear in social contexts may be subserved by different brain regions than fear of inanimate objects.

5. De Bellis MD; Casey BJ; Dahl RE; Birmaher B; Williamson DE; Thomas KM; Axelson DA; Frustaci K; Boring AM; Hall J; Ryan ND.  A pilot study of amygdala volumes in pediatric generalized anxiety disorder. Biol Psychiatry 2000 Jul 1;48(1):51-7 

Abstract:  BACKGROUND: The neurodevelopment of childhood anxiety disorders is not well understood. Basic research has implicated the amygdala and circuits related to these nuclei as being central to several aspects of fear and fear-related behaviors in animals. METHODS: Magnetic resonance imaging was used to measure amygdala volumes and comparison brain regions in 12 child and adolescent subjects with generalized anxiety disorder and 24 comparison subjects. Groups were matched on age, sex, height, and handedness and were also similar on measures of weight, socioeconomic status, and full scale IQ. RESULTS: Right and total amygdala volumes were significantly larger in generalized anxiety disorder subjects. Intracranial, cerebral, cerebral gray and white matter, temporal lobe, hippocampal, and basal ganglia volumes and measures of the midsagittal area of the corpus callosum did not differ between groups. CONCLUSIONS: Although these data are preliminary and from a small sample, the results are consistent with a line of thinking that alterations in the structure and function of the amygdala may be associated with pediatric generalized anxiety disorder.

6. Masaoka Y; Hirasawa K; Yamane F; Hori T; Homma I.  Effects of left amygdala lesions on respiration, skin conductance, heart rate, anxiety, and activity of the right amygdala during anticipation of negative stimulus.  Behav Modif 2003 Oct;27(5):607-19 

Abstract:  The present study reports the effects of lesions in the left amygdala on anxiety, respiration, skin conductance, heart rate, and electrical potentials in the right amygdala in two patients. Trait and anticipatory-state anxiety were measured before and after left amygdala resection to control medically intractable epilepsy in the patients. Lesions in the left amygdala resulted in decreases of trait and state anxiety, respiratory rate, and activity in the right amygdala in both patients; one patient also showed notable decreases in skin conductance and heart rate. The study also reports that activities in the right amygdala before the lesion were not observed after the lesion. We suggest that the activity of the right amygdala is dominantly activated in anxiety and anxiety-related physiological responses but needs excitatory inputs from the left amygdala.

7. Fredrikson M; Furmark T.  Amygdaloid regional cerebral blood flow and subjective fear during symptom provocation in anxiety disorders.  Ann N Y Acad Sci 2003 Apr;985:341-7 

Abstract:  Whether the amygdala is involved predominantly in emotional perception or in the generation of emotional states has been debated. We reviewed and reanalyzed data from our laboratory, indicating that subjective feelings of fear and distress are correlated with regional cerebral blood flow (rCBF) in the right but not the left amygdala during anxiety provocation in individuals with social anxiety disorder, specific phobias. and posttraumatic stress disorder. Positron emission tomography is a correlative technique, and casual inferences cannot be drawn. However, because studies demonstrate that treatment of social anxiety disorder with cognitive behavior therapy and selective serotonin reuptake inhibitors results in reduced rCBF in the amygdaloid complex and prospective studies reveal that treatment-induced alterations in amygdala rCBF can predict 1 year follow-up status in social anxiety disorder data support the notion that the amygdala, at least in part, seem casually involved in generating the subjective experience of fear.

8. Freudenreich, O.; Murray, G. B.  Anxiety and position-dependent neurologic findings due to autonomic dysreflexia.  2001 Psychosomatics  42 (1) 81-2. 

9. Geiderman, J. M.  Sympathetic dystrophy.  2001  Ann Emerg Med  37 (4) 412-4

10. Martinez-Lavin, M.  Is fibromyalgia a generalized reflex sympathetic dystrophy?  2001  Clin Exp Rheumatol  19 (1)  1-3.

Abstract:  Fibromyalgia and reflex sympathetic dystrophy share defining characteristics, namely chronic pain and allodynia, as well as other important clinical features such as onset after trauma, female predominance, paresthesias, vasomotor instability, response to sympathetic blockade and anxiety/depression. Recent research using heart rate variability analysis demonstrated that patients with fibromyalgia have changes consistent with relentless circadian sympathetic hyperactivity. I propose that fibromyalgia is a sympathetically maintained pain syndrome in which ongoing sympathetic hyperactivity sensitises the primary nociceptors and induces widespread pain and allodynia.